ArticlePLoS biology2024
Pharmacological induction of autophagy reduces inflammation in macrophages by degrading immunoproteasome subunits.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Respiratory syncytial virus-induced SIGLEC1 upregulation inhibits macrophage autophagy and facilitates inflammatory mediator secretion.BMJ open respiratory research · 2026Article
- Autophagy-Mitophagy Pathway-Linked Genetic Variants Associate with Systemic Inflammation and Interact with Dietary Factors in Asian and European Cohorts.International journal of molecular sciences · 2026Article
- Amblyomma cajennense Sensu Stricto (Fabricius, 1787) and Amblyomma sculptum (Berlese, 1888) Tick Saliva Elicit Immune-Modulatory Activity in Isolated Murine Macrophages With an Insight Into Proteomic Analysis.Parasite immunology · 2026Article
- Emerging role of the immunoproteasome as a druggable target in lung inflammatory diseases.Respiratory research · 2026Review
- Targeted autophagy: research progress on the regulatory potential of periodontitis prevention and treatment.Frontiers in cell and developmental biology · 2026Review
- Autophagy in tuberculosis: advances, translational gaps, and the promise of host-directed therapies.Frontiers in cellular and infection microbiology · 2026Review
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- Autophagy in Acute Lung Injury.Cell biochemistry and biophysics · 2025Review
- Autophagy and Its Association with Macrophages in Clonal Hematopoiesis Leading to Atherosclerosis.International journal of molecular sciences · 2025Review
- NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.Frontiers in immunology · 2025Review
- Quercetin ameliorates oxidative stress-induced apoptosis of granulosa cells in dairy cow follicular cysts by activating autophagy via the SIRT1/ROS/AMPK signaling pathway.Journal of animal science and biotechnology · 2024Article
- Article
- Article
- Degrade to stay healthy-Proteolytic interplay during inflammation.PLoS biology · 2024Article
- Fibroblast growth factor signaling in macrophage polarization: impact on health and diseases.Frontiers in immunology · 2024Review
- The FGFR inhibitor Rogaratinib reduces microglia reactivity and synaptic loss in TBI.Frontiers in immunology · 2024Article
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7 authors at 3 institutions in 1 country.
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Abstract
Defective autophagy is linked to proinflammatory diseases. However, the mechanisms by which autophagy limits inflammation remain elusive. Here, we found that the pan-FGFR inhibitor LY2874455 efficiently activated autophagy and suppressed expression of proinflammatory factors in macrophages stimulated by lipopolysaccharide (LPS). Multiplex proteomic profiling identified the immunoproteasome, which is a specific isoform of the 20s constitutive proteasome, as a substrate that is degraded by selective autophagy. SQSTM1/p62 was found to be a selective autophagy-related receptor that mediated this degradation. Autophagy deficiency or p62 knockdown blocked the effects of LY2874455, leading to the accumulation of immunoproteasomes and increases in inflammatory reactions. Expression of proinflammatory factors in autophagy-deficient macrophages could be reversed by immunoproteasome inhibitors, confirming the pivotal role of immunoproteasome turnover in the autophagy-mediated suppression on the expression of proinflammatory factors. In mice, LY2874455 protected against LPS-induced acute lung injury and dextran sulfate sodium (DSS)-induced colitis and caused low levels of proinflammatory cytokines and immunoproteasomes. These findings suggested that selective autophagy of the immunoproteasome was a key regulator of signaling via the innate immune system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.